Obesity and type 2 diabetes are diseases of insufficient or deficient regulation. We know from human studies that the small intestine plays a critical role in both energy and glucose homeostasis: when the duodenum is exposed to lipids, appetite is diminished and native (liver) glucose production is down-regulated. Previously we have invented a device that can be implanted into the duodenum and remain in place; we have described devices and methods for slowing the passage of food through the duodenum to cause increased tissue-nutrient contact, thereby causing amplified hormonal signaling from the duodenum; and, we have invented methods and devices for delivering chemicals, drugs or other compounds to the duodenum.
What is needed are devices and/or methods for additional lipid uptake, delaying ingesta passage/prolonging ingesta contact, delivering or providing lipids or other appetite and glucose reducing nutrients and/or combinations of these characteristics.